In a normal heart, cells of the sinoatrial node (SA node) spontaneously depolarize and thereby initiate an action potential. This action potential propagates rapidly through the atria (which contract), slowly through the atrioventricular node (AV node), the atrioventricular bundle (AV bundle or His bundle) and then to the ventricles, which causes ventricular contraction. This sequence of events is known as normal sinus rhythm (NSR). Thus, in a normal heart, ventricular rhythm relies on conduction of action potentials through the AV node and AV bundle.
Rhythms that do not follow the sequence of events described above are known as arrhythmias. Arrhythmias that result in a heart rate slower than normal are called bradyarrhythmias, which are also known as bradycardias. Arrhythmias that result in a faster heart rate than normal are called tachyarrhythmias, which are also known as tachycardias. Tachycardias are further classified as supraventricular or ventricular. Supraventricular tachycardias (SVTS) are characterized by abnormal rhythms that may originate in the atria, the atrioventricular node (AV node), or in the pulmonary veins. For example, a paroxysmal SVT can exhibit heart rates between approximately 140 beats per minute (bpm) and approximately 250 bpm. However, the most common SVTs are typically atrial flutter (AFI) and atrial fibrillation (AF). In addition, many SVTs involve the AV node, for example, AV nodal reentry tachycardia (AVNRT) where an electrical loop or circuit includes the AV node.
Atrial flutter (AFI) can result when an early beat triggers a “circus circular current” that travels in regular cycles around the atrium, pushing the atrial rate up to approximately 250 bpm to approximately 350 bpm. The atrioventricular node between the atria and ventricles will often block one of every two beats, keeping the ventricular rate at about 125 bpm to about 175 bpm. This is the pulse rate that will be felt, even though the atria are beating more rapidly. At this pace, the ventricles will usually continue to pump blood relatively effectively for many hours or even days. A patient with underlying heart disease, however, may experience chest pain, faintness, or even heart failure as a result of the continuing increased stress on the heart muscle. In some individuals, the ventricular rate may also be slower if there is increased block of impulses in the AV node, or faster if there is little or no block.
If the cardiac impulse fails to follow a regular circuit and divides along multiple pathways, a chaos of uncoordinated beats results, producing atrial fibrillation (AF). AF commonly occurs when the atrium is enlarged (usually because of heart disease). In addition, it can occur in the absence of any apparent heart disease. In AF, the atrial rate can increase to more than 350 bpm and cause the atria to fail to pump blood effectively. Under such circumstances, the ventricular beat may also become haphazard, producing a rapid irregular pulse. Although AF may cause the heart to lose approximately 20 to 30 percent of its pumping effectiveness, the volume of blood pumped by the ventricles usually remains within the margin of safety, again because the atrioventricular node blocks out many of the chaotic beats. Hence, during AF, the ventricles may contract at a lesser rate than the atria, for example, of approximately 125 bpm to approximately 175 bpm.
Overall, SVTs are typically not immediately life threatening when compared to ventricular arrhythmias, examples of which are discussed below. SVTs can typically be left untreated for long periods of time without significant harm to the patient.
Ventricular arrhythmias, which originate in the ventricles, include ventricular tachycardia (VT) and ventricular fibrillation (VF). Ventricular arrhythmias are often associated with rapid and/or chaotic ventricular rhythms. For example, sustained VT can lead to VF. In sustained VT, consecutive impulses arise from the ventricles at a rate of 100 bpm or more. Such activity may degenerate further into disorganized electrical activity, known as VF. In VF, disorganized action potentials can cause the myocardium to quiver rather than contract. Such chaotic quivering can greatly reduce the heart's pumping ability. Indeed, approximately two-thirds of all deaths from arrhythmia are caused by VF. A variety of conditions such as, but not limited to, hypoxia, ischemia, pharmacologic therapy (e.g., sympathomimetics), and asynchronous pacing may promote onset of ventricular arrhythmia.
VF is typically fatal if not terminated within minutes using shock therapy. VT can be lethal if not treated promptly, and is usually treated using either anti-tachycardia pacing (ATP) or shock therapy to terminate an episode of VT.
It has been common practice for an implantable cardioverter defibrillator (ICD) to monitor heart rate, or more commonly the ventricular rate, of a patient and classify the cardiac condition of the patient based on this heart rate. For example, a tachyarrhythmia may be defined as any rate in a range above a designated threshold. This range is then divided into ventricular tachycardia and ventricular fibrillation zones. The ventricular tachycardia zone may be further divided into slow ventricular tachycardia and fast ventricular tachycardia zones.
As described above, SVTs and ventricular arrhythmias may lead to ventricular rates in excess of 100 bpm. In other words, ventricular rates of SVTs can overlap with rates of tachycardias of ventricular origin. These SVTs are often well tolerated and require no intervention. Further, physically active patients can have heart rates during exercise that overlap with their tachycardia rates. Accordingly, discrimination of VT from SVT may require more than just knowledge of a patient's ventricular rate. In other words, using heart rate as the sole criterion to diagnose the cardiac condition of a patient is often not sufficient.
To improve device diagnoses, many implantable cardiac devices can also examine the morphology of an intracardiac electrogram (EGM) and/or electrocardiogram (ECG), in addition to the heart rate. The shape of an intracardiac complex can include information on the origin and sequence of the heart's electrical activity. A normal intracardiac complex traverses the AV node and is conducted by specialized cardiac tissue throughout the ventricles. This results in a distinctive complex morphology. A tachycardia of ventricular origin often has a different morphology due to its ectopic origin and conductance through cardiac muscle tissue. As such, in addition to monitoring heart rate, some implantable cardiac devices are capable of performing morphology discrimination to classify the cardiac condition of the patient (i.e., to produce a device diagnosis). For example, a template based on the morphology of a “known” signal can be stored in the implantable cardiac device. The “known” signal can be, for example, a signal collected during a period where a patient is known to exhibit a normal sinus rhythm. By comparing the morphology characteristics (e.g., number, amplitude, sequence and/or polarity of waveform peaks, as well as the area under the peaks) of an arrhythmia to the template, the implantable cardiac device can calculate the match between the waveforms. For a further description of morphology discrimination, refer to U.S. Pat. No. 5,240,009 (Williams), entitled “Medical Device with Morphology Discrimination” and to U.S. Pat. No. 5,779,645 (Olson et al.), entitled “System and Method for Waveform Morphology Comparison,” which patents are hereby incorporated by reference. For more specific examples, a morphology percentage match threshold and/or a number of matches in a given window can be defined. These are just a few examples of morphology discriminators, which are not intended to be limiting.
Sudden onset and interval stability (also know as rate stability), which are discussed in more detail below, are examples of other factors that can be monitored to improve device diagnoses. Also, the relationship between ventricular rate (V) and atrial rate (A) can be used. For example, this can be part of a rate branch algorithm, which, depending on V and A, may follow one of three branches: a V<A rate branch; a V=A (within a specified tolerance) rate branch; and a V>A rate branch. If V<A, then morphology discrimination and/or interval stability may be available to distinguish VT from AF or AFI. If A and V are essentially the same (within a certain tolerance), then morphology discrimination and/or sudden onset may be available to distinguish VT from sinus tachycardia. If V>A, then an arrhythmia may be characterized as VT. Also, specific branches can be turned on or off. For example, if V is greater than the tachycardia threshold but essentially the same as A, and the V=A branch is turned off, then the algorithm can cause the V>A branch to be followed, and the arrhythmia may be classified as VT. Additional details of an exemplary rate branch algorithm are provided in U.S. Pat. No. 6,636,764 (Fain et al.), entitled “Safety Backup in Arrhythmia Discrimination Algorithm,” which is incorporated herein by reference. Atrioventricular association (AVA) can also be used to distinguish AFI from VT. In an exemplary (AVA) algorithm, the AV interval is measured from each ventricular sensed event to its preceding atrial event and an AVA Delta is then calculated as the difference between the second longest AV interval and the second shortest AV interval in a recent group of intervals. If the measured AVA Delta is less than a programmable AVA threshold parameter, the AV intervals are considered stable, which is indicative of SVT. If the measured AVA Delta is greater than or equal to a programmable AVA threshold parameter, the AV intervals are considered unstable, which is indicative of VT. More generally, discriminators relating to the relative rate of the atria and ventricles and/or the timing relationship between atrial and ventricular events can be used to produce device diagnoses.
An implantable cardiac device can be programmed to provide a therapy in response to an arrhythmia being detected, where the type of therapy corresponds to the type of arrhythmia that the device believes it has detected (the arrhythmia the device believes it has detected can be referred to as the device diagnosis). For example, VT may be treated with a therapy consisting of low-energy pacing pulses designed to capture the ventricles. This therapy is referred to as Anti-Tachycardia Pacing therapy (ATP). VT may also be treated with relatively low energy, synchronized cardioversion shocks. VF, on the other hand, is typically treated more aggressively with high energy shocks. The implantable cardiac device is programmed with numerous parameters that are used to discriminate between types of arrhythmias, and to define the types of therapies to be used to treat the various arrhythmias. An SVT may or may not be treated, depending on how the implantable cardiac device is programmed.
Over the years, the number of programmable arrhythmia discriminators has increased. A major challenge for both implantable cardiac device manufacturers and caregivers (e.g., physicians, clinicians, and the like) is to select proper uses of these discriminators and values of parameters of theses discriminators. While a manufacturer may provide nominal values of parameters and uses of these discriminators, these nominal values and uses (also referred to as default values and uses) may not be proper for all patients, and it is up to the caregiver to change them, e.g., using statistical information, knowledge of the patient and his/her condition, and the caregiver's personal experience.
Caregivers often have difficulty programming discriminators intended to aid in the discrimination of tachycardias (e.g., SVT from VT), because the implications of making adjustments to discriminators are often not readily clear. As a result, caregivers often do not turn on certain discriminators routinely, waiting to see if the patient will receive inappropriate therapies before attempting to reprogram the device appropriately, or caregivers turn the discriminators on with the default parameter values provided by the manufacturer, without any attempt to customize them for the individual needs of the patient.
As can be appreciated from the above description, implantable cardiac devices face the difficult challenge of appropriately discriminating between different types of arrhythmias, such as VT and SVT. Several discrimination algorithms exist that rely on discriminators to differentiate such arrhythmias. However, appropriate programming of these algorithms, including the appropriate selection of parameter values and uses of specific discriminators, can be challenging due to algorithm complexity, patient to patient variability, change in patient condition, and lack of information available to the caregiver at the time of the device implant. Accordingly, there is still a need to assist physicians, clinicians and other caregivers (generally referred to as users) in programming discriminators in a way more appropriate to the indications and characteristics of individual patients. More generally, there is still a need to improve how implantable cardiac devices are programmed to perform arrhythmia discrimination.